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https://www.readbyqxmd.com/read/29039493/actein-induces-apoptosis-in-leukemia-cells-through-suppressing-rhoa-rock1-signaling-pathway
#1
Wen-Di Zhou, Xiang Wang, Xing-Zhen Sun, Jian Hu, Rong-Rong Zhang, Ze Hong
Actein is a tetracyclic triterpenoid compound, extracted from the rhizome of Cimicifuga foetida, exhibiting anticancer activities as previously reported. However, the effects of actein on human leukemia have not been explored before. In this study, the role of actein in regulating apoptosis induction in human leukemia cells was investigated. Actein administration significantly enhanced apoptosis, especially in human leukemia cell line of U937 and the primary human leukemia cells. The promotion was accompanied by caspase-9, caspase-3 and poly(ADP-ribose) polymerase (PARP) cleavage, and cytochrome c (Cyto-c) release...
October 10, 2017: International Journal of Oncology
https://www.readbyqxmd.com/read/28977846/downregulation-of-x-linked-inhibitor-of-apoptosis-protein-by-7-benzylidenenaltrexone-maleate-sensitizes-pancreatic-cancer-cells-to-trail-induced-apoptosis
#2
So Young Kim, Sojung Park, SeonA Yoo, Jin Kyung Rho, Eun Sung Jun, Suhwan Chang, Kyung Kon Kim, Song Cheol Kim, Inki Kim
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potential biological anticancer agent. However, a wide range of human primary cancers, including pancreatic cancer, display resistance to apoptosis induction by TRAIL. Therefore, this resistance needs to be overcome to allow TRAIL to be successfully used in cancer therapy. In this study, we performed a compound screen to isolate TRAIL sensitizers and found that one of the identified compounds, 7-benzylidenenaltrexone maleate (BNTX), sensitized pancreatic cancer cells to TRAIL-induced apoptotic cell death...
September 22, 2017: Oncotarget
https://www.readbyqxmd.com/read/28973175/amyotrophic-lateral-sclerosis-associated-mutant-sod1-inhibits-anterograde-axonal-transport-of-mitochondria-by-reducing-miro1-levels
#3
Annekathrin Moller, Claudia S Bauer, Rebecca N Cohen, Christopher P Webster, Kurt J De Vos
Defective axonal transport is an early neuropathological feature of amyotrophic lateral sclerosis (ALS). We have previously shown that ALS-associated mutations in Cu/Zn superoxide dismutase 1 (SOD1) impair axonal transport of mitochondria in motor neurons isolated from SOD1 G93A transgenic mice and in ALS mutant SOD1 transfected cortical neurons, but the underlying mechanisms remained unresolved.The outer mitochondrial membrane protein mitochondrial Rho GTPase 1 (Miro1) is a master regulator of mitochondrial axonal transport in response to cytosolic calcium (Ca2+) levels ([Ca2+]c) and mitochondrial damage...
September 14, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28712398/-fasudil-attenuates-mitochondrial-injury-and-apoptosis-in-rat-model-of-myocardial-ischemia-reperfusion-injury
#4
Hongwei Ye, Guanjun Zhang, Ruiping Cao, Pinfang Kang, Zhenghong Li, Qin Gao
Objective To observe the changes of mitochondria fusion protein 2 (Mfn2) and dynamin-related protein 1 (Drp1) in the cardioprotection of fasudil, and analyze the significance. Methods Hearts isolated from male Sprague-Dawley rats were subjected to ischemia for 30 minutes (occlusion of left anterior descending artery), and continuously perfusion for 120 minutes to establish myocardial ischemia/reperfusion (I/R) injury model. The rats were divided into 3 groups: sham group, I/R group and fasudil group. The left ventricular hemodynamics were continuously recorded; lactate dehydrogenase (LDH) content was measured during reperfusion; myocardial ultrastructure was observed by electron microscopy; the protein expression of phosphorylated protein phosphatase 1 regulatory subunit 12A (p-PPP1R12A/p-MYPT1) was detected by immunohistochemistry; and the protein expressions of Mfn2, Drp1 and cleaved caspase-3 (c-caspase-3) were detected by Western blot analysis...
July 2017: Xi Bao Yu Fen Zi Mian Yi Xue za Zhi, Chinese Journal of Cellular and Molecular Immunology
https://www.readbyqxmd.com/read/28521307/downregulation-of-x-linked-inhibitor-of-apoptosis-protein-by-7-benzylidenenaltrexone-maleate-sensitizes-pancreatic-cancer-cells-to-trail-induced-apoptosis
#5
So Young Kim, Sojung Park, SeonA Yoo, Jin Kyung Rho, Eun Sung Jun, Suhwan Chang, Kyung Kon Kim, Song Cheol Kim, Inki Kim
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potential biological anticancer agent. However, a wide range of human primary cancers, including pancreatic cancer, display resistance to apoptosis induction by TRAIL. Therefore, this resistance needs to be overcome to allow TRAIL to be successfully used in cancer therapy. In this study, we performed a compound screen to isolate TRAIL sensitizers and found that one of the identified compounds, 7-benzylidenenaltrexone maleate (BNTX), sensitized pancreatic cancer cells to TRAIL-induced apoptotic cell death...
May 12, 2017: Oncotarget
https://www.readbyqxmd.com/read/28409271/unique-presentation-of-cutis-laxa-with-leigh-like-syndrome-due-to-echs1-deficiency
#6
S Balasubramaniam, L G Riley, D Bratkovic, D Ketteridge, N Manton, M J Cowley, V Gayevskiy, T Roscioli, M Mohamed, T Gardeitchik, E Morava, J Christodoulou
Clinical finding of cutis laxa, characterized by wrinkled, redundant, sagging, nonelastic skin, is of growing significance due to its occurrence in several different inborn errors of metabolism (IEM). Metabolic cutis laxa results from Menkes syndrome, caused by a defect in the ATPase copper transporting alpha (ATP7A) gene; congenital disorders of glycosylation due to mutations in subunit 7 of the component of oligomeric Golgi (COG7)-congenital disorders of glycosylation (CDG) complex; combined disorder of N- and O-linked glycosylation, due to mutations in ATPase H+ transporting V0 subunit a2 (ATP6VOA2) gene; pyrroline-5-carboxylate reductase 1 deficiency; pyrroline-5-carboxylate synthase deficiency; macrocephaly, alopecia, cutis laxa, and scoliosis (MACS) syndrome, due to Ras and Rab interactor 2 (RIN2) mutations; transaldolase deficiency caused by mutations in the transaldolase 1 (TALDO1) gene; Gerodermia osteodysplastica due to mutations in the golgin, RAB6-interacting (GORAB or SCYL1BP1) gene; and mitogen-activated pathway (MAP) kinase defects, caused by mutations in several genes [protein tyrosine phosphatase, non-receptor-type 11 (PTPN11), RAF, NF, HRas proto-oncogene, GTPase (HRAS), B-Raf proto-oncogene, serine/threonine kinase (BRAF), MEK1/2, KRAS proto-oncogene, GTPase (KRAS), SOS Ras/Rho guanine nucleotide exchange factor 2 (SOS2), leucine rich repeat scaffold protein (SHOC2), NRAS proto-oncogene, GTPase (NRAS), and Raf-1 proto-oncogene, serine/threonine kinase (RAF1)], which regulate the Ras-MAPK cascade...
April 13, 2017: Journal of Inherited Metabolic Disease
https://www.readbyqxmd.com/read/28004868/physiological-redox-signalling-and-regulation-of-ion-channels-implications-for-pulmonary-hypertension
#7
Jeremy P T Ward
What is the topic of this review? The review concerns the role of reactive oxygen species as physiological second messengers in potentiating G-protein-coupled receptor-mediated vasoconstriction and its potential dysregulation by oxidant stress in pulmonary hypertension. What advances does it highlight? The review highlights the concept that physiological signalling by reactive oxygen species must normally be highly compartmentalized to prevent self-regenerating oxidant stress and promiscuous and uncontrolled signalling, which contribute to the aetiology...
December 22, 2016: Experimental Physiology
https://www.readbyqxmd.com/read/27930804/increased-mitochondrial-ros-generation-mediates-the-loss-of-the-anti-contractile-effects-of-perivascular-adipose-tissue-in-high-fat-diet-obese-mice
#8
Rafael Menezes da Costa, Rafael S Fais, Carlos R P Dechandt, Paulo Louzada-Junior, Luciane C Alberici, Núbia S Lobato, Rita C Tostes
BACKGROUND AND PURPOSE: Obesity is associated with structural and functional changes in perivascular adipose tissue (PVAT), favouring release of reactive oxygen species (ROS), vasoconstrictor and proinflammatory factors. The cytokine TNF-α induces vascular dysfunction and is produced by PVAT. We tested the hypothesis that obesity-associated PVAT dysfunction was mediated by augmented mitochondrial ROS (mROS) generation due to increased TNF-α production in this tissue. EXPERIMENTAL APPROACH: C57Bl/6J and TNF-α receptor-deficient mice received control or high fat diet (HFD) for 18 weeks...
October 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/27572148/mitochondrial-fission-of-smooth-muscle-cells-is-involved-in-artery-constriction
#9
COMPARATIVE STUDY
Ming-Yu Liu, Jing Jin, Shan-Liang Li, Jie Yan, Chang-Lin Zhen, Jin-Lai Gao, Yong-Hui Zhang, Yan-Qiu Zhang, Xin Shen, Liang-Shuan Zhang, Yuan-Yuan Wei, Yu Zhao, Chen-Guang Wang, Yun-Long Bai, De-Li Dong
Mitochondria are dynamic organelles and continuously undergo fission and fusion processes. Mitochondrial fission is involved in multiple physiological or pathological processes, but the role of mitochondrial fission of smooth muscle cells in artery constriction is unknown. The role of mitochondrial fission of smooth muscle cells in arterial function was investigated by measuring the tension of rat mesenteric arteries and thoracic aorta and by evaluating mitochondrial fission, mitochondrial reactive oxygen species, and cytosolic [Ca(2+)]i in rat vascular smooth muscle cells...
November 2016: Hypertension
https://www.readbyqxmd.com/read/27563890/antiviral-activity-of-a-novel-compound-cw-33-against-japanese-encephalitis-virus-through-inhibiting-intracellular-calcium-overload
#10
Su-Hua Huang, Jin-Cherng Lien, Chao-Jung Chen, Yu-Ching Liu, Ching-Ying Wang, Chia-Fong Ping, Yu-Fong Lin, An-Cheng Huang, Cheng-Wen Lin
Japanese encephalitis virus (JEV), a mosquito-borne flavivirus, has five genotypes (I, II, III, IV, and V). JEV genotype I circulates widely in some Asian countries. However, current JEV vaccines based on genotype III strains show low neutralizing capacities against genotype I variants. In addition, JE has no specific treatment, except a few supportive treatments. Compound CW-33, an intermediate synthesized derivative of furoquinolines, was investigated for its antiviral activities against JEV in this study...
August 24, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/26602979/endotoxemia-engages-the-rhoa-kinase-pathway-to-impair-cardiac-function-by-altering-cytoskeleton-mitochondrial-fission-and-autophagy
#11
Sebastien Preau, Florian Delguste, Yichi Yu, Isabelle Remy-Jouet, Vincent Richard, Fabienne Saulnier, Eric Boulanger, Remi Neviere
AIMS: The RhoA/ROCK pathway controls crucial biological processes involved in cardiovascular pathophysiology, such as cytoskeleton dynamics, vascular smooth muscle contraction, and inflammation. In this work, we tested whether Rho kinase inhibition would beneficially impact cardiac cytoskeleton organization, bioenergetics, and autophagy in experimental endotoxemia induced by lipopolysaccharides (LPSs) in mice. RESULTS: Fasudil, a potent ROCK inhibitor, prevented LPS-induced cardiac inflammation, oxidative stress, cytoskeleton disarray, and mitochondrial injury...
April 1, 2016: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/26464714/effect-of-fasudil-on-hypoxic-pulmonary-hypertension-and-right-ventricular-hypertrophy-in-rats
#12
Xing-Zhen Sun, Shu-Yan Li, Xiang-Yang Tian, Qing-Quan Wu
OBJECTIVE: To investigate whether right ventricular hypertrophy in hypoxic pulmonary hypertension (HPH) rats could be prevented by treatment with Rho kinase inhibitor fasudil. METHODS: The rat model of pulmonary hypertension was established by exposing rats to normobaric intermitent hypoxia [(10 ± 0.5)% O2]. Twenty-four Spraque-Dawley male rats were randomly divided into control group, hypoxic model group and hypoxia with fasudil groups (n=8 each). The mean pulmonary arterial pressure (mPAP), and right ventricle hypertrophy index (RVHI) were measured...
2015: International Journal of Clinical and Experimental Pathology
https://www.readbyqxmd.com/read/26187664/l-f001-a-multifunctional-rock-inhibitor-prevents-paraquat-induced-cell-death-through-attenuating-er-stress-and-mitochondrial-dysfunction-in-pc12%C3%A2-cells
#13
Wei Shen, Lan Wang, Rongbiao Pi, Zhifeng Li, Rikang Wang
Paraquat (PQ) was demonstrated to induce dopaminergic neuron death and is used as a Parkinson's disease (PD) mimetic. Amounting evidences demonstrated that Rho/ROCK may a novel target for the therapy of PD. Previously we synthesized L-F001 and proved it is a potent ROCK inhibitor with multifunctional effects, including anti-oxidative stress. In this study, we investigated the effects and also the molecular mechanisms of L-F001 in preventing PQ-induced cytotoxicity in PC12 cells. L-F001 effectively prevented PQ-induced apoptotic cell death, which involves the scavenger of ROS and also attenuated the declined of mitochondrial membrane potential and intracellular level of GSH induced by PQ...
August 28, 2015: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/26169112/role-of-rho-kinase-inhibition-in-the-protective-effect-of-fasudil-and-simvastatin-against-3-nitropropionic-acid-induced-striatal-neurodegeneration-and-mitochondrial-dysfunction-in-rats
#14
Lamiaa A Ahmed, Hebatallah A Darwish, Rania M Abdelsalam, HebatAllah A Amin
3-Nitropropionic acid (3-NP)-induced neurotoxicity is an experimental model which mimics the pathology and motor abnormalities seen in Huntington's disease (HD) in human. The present investigation was directed to estimate the role of rho kinase (ROCK) inhibition in the possible protective effect of fasudil and simvastatin in 3-NP-induced striatal neurodegeneration in rats. Animals were injected s.c. with 3-NP (20 mg/kg/day) for 1 week with or without administration of fasudil (10 mg/kg/day, p.o.) or simvastatin (20 mg/kg/day, p...
August 2016: Molecular Neurobiology
https://www.readbyqxmd.com/read/25969509/defining-roles-of-parkin-and-ubiquitin-phosphorylation-by-pink1-in-mitochondrial-quality-control-using-a-ubiquitin-replacement-strategy
#15
Alban Ordureau, Jin-Mi Heo, David M Duda, Joao A Paulo, Jennifer L Olszewski, David Yanishevski, Jesse Rinehart, Brenda A Schulman, J Wade Harper
The PTEN-induced putative kinase protein 1 (PINK1) and ubiquitin (UB) ligase PARKIN direct damaged mitochondria for mitophagy. PINK1 promotes PARKIN recruitment to the mitochondrial outer membrane (MOM) for ubiquitylation of MOM proteins with canonical and noncanonical UB chains. PINK1 phosphorylates both Ser65 (S65) in the UB-like domain of PARKIN and the conserved Ser in UB itself, but the temporal sequence and relative importance of these events during PARKIN activation and mitochondria quality control remain poorly understood...
May 26, 2015: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/25892241/compartmentalized-ampk-signaling-illuminated-by-genetically-encoded-molecular-sensors-and-actuators
#16
Takafumi Miyamoto, Elmer Rho, Vedangi Sample, Hiroki Akano, Masaki Magari, Tasuku Ueno, Kirill Gorshkov, Melinda Chen, Hiroshi Tokumitsu, Jin Zhang, Takanari Inoue
AMP-activated protein kinase (AMPK), whose activity is a critical determinant of cell health, serves a fundamental role in integrating extracellular and intracellular nutrient information into signals that regulate various metabolic processes. Despite the importance of AMPK, its specific roles within the different intracellular spaces remain unresolved, largely due to the lack of real-time, organelle-specific AMPK activity probes. Here, we present a series of molecular tools that allows for the measurement of AMPK activity at the different subcellular localizations and that allows for the rapid induction of AMPK inhibition...
April 28, 2015: Cell Reports
https://www.readbyqxmd.com/read/25868250/-ck2beta-promotes-pink1-parkin-mediated-miro1-degradation
#17
Chenliang Zhang, Siyue Qin, Chang'an Jiang
PTEN-induced putative kinase 1 (PINK1), a Parkinson's disease (PD)-related protein, has two isoforms, the mitochondria-localized full-length isoform PINK1FL and the cytoplasm-localized short isoform PINK1-cyto. Studies have suggested that PINK1FL can selectively accumulate at the surface of damaged mitochondria and cooperate with another Parkinson's Disease-related protein PARKIN to trigger the degradation of MIRO1, a mitochondria trafficking regulator. The functions of PINK1-cyto are, however, not yet clear...
December 2014: Sheng Wu Yi Xue Gong Cheng Xue za Zhi, Journal of Biomedical Engineering, Shengwu Yixue Gongchengxue Zazhi
https://www.readbyqxmd.com/read/25752214/beneficial-effect-of-cyclosporine-a-on-traumatic-hemorrhagic-shock
#18
Yan Lei, Xiaoyong Peng, Liangming Liu, Zhaojun Dong, Tao Li
BACKGROUND: Vascular hyporeactivity plays an important role in severe trauma and shock. We investigated the beneficial effect of cyclosporine A (CsA) on traumatic shock and its relationship to vascular reactivity improvement and mitochondrial permeability transition pore (MPTP). MATERIALS AND METHODS: Sodium pentobarbital-anesthetized rats were used to induce traumatic hemorrhagic shock by left femur fracture and hemorrhage, the beneficial effects of CsA (1, 5, and 10 mg/kg, intravenously) on animal survival, cardiovascular function, tissue blood perfusion, and mitochondrial function of vital organs were observed...
May 15, 2015: Journal of Surgical Research
https://www.readbyqxmd.com/read/25520072/ursolic-acid-promotes-apoptosis-of-sgc-7901-gastric-cancer-cells-through-rock-pten-mediated-mitochondrial-translocation-of-cofilin-1
#19
Rui Li, Xia Wang, Xiao-Hong Zhang, Hong-Hai Chen, Yan-Dong Liu
Ursolic acid, extracted from the traditional Chinese medicine bearberry, can induce apoptosis of gastric cancer cells. However, its pro-apoptotic mechanism still needs further investigation. More and more evidence demonstrates that mitochondrial translocation of cofilin-1 appears necessary for the regulation of apoptosis. Here, we report that ursolic acid (UA) potently induces the apoptosis of gastric cancer SGC-7901 cells. Further mechanistic studies revealed that the ROCK1/PTEN signaling pathway plays a critical role in UA-mediated mitochondrial translocation of cofilin-1 and apoptosis...
2014: Asian Pacific Journal of Cancer Prevention: APJCP
https://www.readbyqxmd.com/read/25380156/c-src-erk1-2-and-rho-kinase-mediate-hydrogen-peroxide-induced-vascular-contraction-in-hypertension-role-of-txa2-nad-p-h-oxidase-and-mitochondria
#20
Ana B García-Redondo, Ana M Briones, Sonia Martínez-Revelles, Teresa Palao, Luis Vila, María J Alonso, Mercedes Salaices
AIM: : The aim of this study was to analyse the signalling pathways involved in H2O2 vascular responses in hypertension. METHODS: Vascular function, thromboxane A2 (TXA2) production, oxidative stress and protein expression were determined in mesenteric resistance arteries (MRAs) from hypertensive (spontaneously hypertensive rats, SHR) and normotensive Wistar Kyoto (WKY) rats. RESULTS: H2O2 and the TP agonist U46619 induced greater contractile responses in MRA from SHR than WKY...
January 2015: Journal of Hypertension
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